Testosterone is a major factor responsible for the greater Denervation, Reinnervation,  muscle mass in men because it has both myotrophic action ). A variety of synthetic molecules, called anabolic steroids, As already noted, innervation is crucial for the skeletal have been designed to enhance muscle growth while mini-muscle phenotype. If the motor nerve is cut, muscle fasmizing their androgenic action. These drugs are widely used ciculation occurs. Fasciculation is characterized by small, by bodybuilders and athletes in sports in which strength is irregular contractions caused by release of acetylcholine from important. The doses are typically 10-to 50-fold greater the terminals of the degenerating distal portion of the axon. than might be prescribed therapeutically for individuals Several days after denervation, muscle fibrillation begins. with impaired hormone production. Unfortunately, none Fibrillation is characterized by spontaneous, repetitive of these compounds lack androgenic effects. Hence, at the contractions. At this time, the cholinergic receptors have doses used, they induce serious hormone disturbances, spread out over the entire cell membrane, in effect reverting including depression of testosterone production. A major to their preinnervation embryonic arrangement. The muscle issue is whether these drugs do in fact increase muscle and fibrillations reflect supersensitivity to acetylcholine. Affected athletic performance in individuals with normal circulating muscles also atrophy, with a decrease in the size of the levels of testosterone. Although they have been used since muscle and its cells. Atrophy is progressive in humans, with the 1950s, the scientific facts remain uncertain, and most degeneration of some cells 3 or 4 months after denervation. experimental studies in animals have not demonstrated Most of the muscle fibers are replaced by fat and connective any significant effects on muscle development. Reports of tissue after 1 to 2 years. These changes can be reversed if studies in humans remain controversial. Proponents claim reinnervation occurs within a few months. Reinnervation increases in strength that provide advantages in world-class is normally achieved by growth of the peripheral stump of performance. Critics argue that these increases are largely motor nerve axons along the old nerve sheath. placebo effects associated with expectations and motivational Reinnervation of formerly fast (type II) fibers by a small factors. The public debate on abuse of anabolic steroids has motor axon causes that cell to redifferentiate into a slow led to their designation as controlled substances, along with (type I) fiber, and vice versa. This suggests that large and opiates, amphetamines, and barbiturates. small motor nerves differ qualitatively and that the nerves have a specific “trophic” effect on the muscle fibers. This “trophic” effect reflects the rate of fiber stimulation. For example, stimulation via electrodes implanted in the muscle can lessen denervation atrophy. More strikingly, chronic low-frequency stimulation of fast motor units causes these units to be converted to slow units. Some conversion toward a typical fast-fiber phenotype can occur when the frequency of contraction in slow units is greatly decreased by reducing the excitatory input. Excitatory input can be reduced by sectioning the appropriate spinal or dorsal root or by severing the tendon, which functionally inactivates peripheral mechanoreceptors.
The frequency of contraction determines fiber development and phenotype through changes in gene expression and protein synthesis. Fibers that undergo frequent contractile activity form many mitochondria and synthesize the slow isoform of myosin. Fibers innervated by large, less excitable axons contract infrequently. Such relatively inactive fibers typically form few mitochondria, have large concentrations of glycolytic enzymes and synthesize the fast isoform of myosin.